The increased activity of peripheral sympathetic nerves, observed in experimental hypertensive states, has been attributed to an abnormality in the intraneuronal norepinephrine (NE) storage mechanism. The proposed projects examines the adrenergic vesicles of peripheral nerves in three forms of experimental hypertension: DOCA-NaC1 induced, renal and spontaneous hypertension. In order to remove the influence of variations in the flow of nerve impulses, the NE storage capacity of nerve terminals will be studied "in vitro" on heart slices. The "in vitro" accumulation of NE into slices will be used as a functional index of storage ability. In vitro release of labeled NE from heart slices will also be examined in various hypertensive states. The adrenergic vesicles of peripheral neurones will also be investigated by a technique of affinity labeling with tritiated reserpine (H3-R), a specific marker of storage vesicles. H3-R binding studies will provide information on quantitative changes in the adrenergic vesicles population. This study will investigate whether qualitative (functional) or quantitative alterations in the adrenergic vesicles of peripheral neurones occur in various forms of experimental hypertension. Changes in adrenergic vesicles will be followed at various stages of the hypertensive condition in order to discern whether they contribute to the development of the disease or they represent an expression of adaptive phenomena due to the disease.